Download Outline26 Renal2 - Napa Valley College

Biology 219 – Human Physiology
Clemens
Renal Physiology 2 - Fluid and Electrolyte Balance
Text: Ch. 20
A. Osmoregulation (Water Balance)
- involves regulation of body fluid osmolarity (concentration) and total fluid volume
To maintain steady state: water gain = water loss
urine is a major avenue of water loss (~ 1.5 L/day)
kidneys conserve water, control volume and concentration of urine excreted
1. Regulation of ECF Osmolarity
- ECF osmolarity affects H2O movement in and out of cells
ICF
ECF
normal ECF osmolarity = 290 mOsm
H2O → H2O
↑ ECF osmolarity → ↓ ICF volume
←
↓ ECF osmolarity → ↑ ICF volume
hypothalamus - osmoreceptors respond to high plasma osmolarity
neurosecretory cells produce ADH (vasopressin), secreted by posterior pituitary
high ADH levels:
low ADH levels:
↑ permeability of CD to H2O
↓ permeability of CD to H2O
↑
→ H2O reabsorbed from CD
→ ↓ H2O reabsorbed from CD
→ concentrated urine, less H2O lost
→ dilute urine, more H2O lost
(e.g. diabetes insipidus)
Negative feedback control:
↑ ECF osmolarity → ↑ ADH secretion → ↑ H2O reabsorption from CD → ↓ ECF osmolarity
2. Regulation of ECF Volume
- ECF volume affects blood pressure
- kidneys help control ECF volume via:
1. regulation of H2O reabsorption/ excretion - controlled by ADH
2. regulation of solute reabsorption/ excretion
- Na+ and Cl- are the most abundant ECF solutes
- total amount of Na+ in the ECF affects ECF volume
↑ Na+ in ECF → ↑ ECF osmolarity → ↑ ADH → ↑ H2O reabsorption → ↑ ECF volume
Fluid imbalances may involve change in osmolarity, volume, or both.
e.g., hypertonic dehydration: ↑ ECF osmolarity and ↓ ECF volume
isotonic dehydration: ↓ ECF volume with normal ECF osmolarity
B. Electrolyte Balance: Na+ and K+ Regulation
- most Na+ and K+ filtered into nephrons is reabsorbed in the PCT
- regulated reabsorption and secretion of Na+ and K+ in the DCT and upper CD
aldosterone - secreted by the adrenal cortex
- stimulates Na+ reabsorption and K+ secretion in principle (P) cells of DCT and CD
- activates apical Na+ and K+ channels and basolateral Na+-K+ pumps
aldosterone secretion is stimulated by
1. high plasma [K+]
2. renin-angiotensin-aldosterone system: responds to low BP and low [Na+]
juxtaglomerular apparatus
granular (juxtaglomerular) cells - sense BP in afferent arteriole
macula densa - senses [Na+] in tubular fluid
renin - enzyme secreted into blood by granular cells
in blood, renin converts angiotensinogen to angiotensin I
in capillaries, angiotensin converting enzyme (ACE) converts ANG I to ANG II
angiotensin II effects:
1. vasoconstriction →  peripheral resistance →  BP
2. stimulates aldosterone secretion →  Na+ reabsorption →  plasma volume →  BP
C. Renal Acid-Base Regulation
Kidneys control excretion of metabolic (non-CO2) acids and bases
- normally secrete H+ and reabsorb HCO3- rates of H+ secretion and HCO3- reabsorption are adjusted to respond to alterations in
pH and [HCO3-] of the plasma
- net result is regulation of plasma [HCO3-] and pH
Negative feedback control
normal pH = 7.4 and [HCO3-] = 24 mM
 [HCO3-] and/or  pH →  H+ secretion and  HCO3- reabsorption →  [HCO3-],  pH
 [HCO3-] and/or  pH →  H+ secretion and  HCO3- reabsorption →  [HCO3-],  pH
Mechanism of bicarbonate reabsorption
1. HCO3- in tubular fluid (PCT and DCT) combines with H+ to form CO2 + H2O
(catalyzed by carbonic anhydrase in the tubule)
2. CO2 diffuses into the tubule epithelial cells
3. CO2 is converted to H+ + HCO3- (via carbonic anhydrase inside the cell)
4. HCO3- is transported to ECF,
H+ is pumped back out to the tubule lumen